T cell responses must adequately defend against pathogens but should terminate once they have eliminated the pathogen that elicited them. In the absence of this control, lymphoproliferation would continue unabated and antithetically would destroy the host. T cell responses are regulated by dendritic cells (DCs) which are educated by the local factors they sense. It is widely accepted that toll like receptor (TLR) signaling triggered by pathogen components educates them to initiate T effector cell responses. This process, in large part, involves upregulation of their MHC class II and B7/CD40 costimulatory molecule expression. The absence of TLR signals in conjunction with locally produced immunosuppressive cytokines educates DCs to extinguish T cell responses by producing T regulatory (Treg) cells. Central among these cells are antigen specific (induced) FoxP3+ Treg cells. In conjunction with nuclear expression of the forkhead/winged-helix family transcription factor (TF) member, FoxP3, these cells surface express CD25, the α chain of the IL-2 receptor (IL-2R) which greatly augments its affinity for IL-2, and CTLA-4, a potent inhibitor of B7 induced CD28 signaling in T effectors needed both for their proliferation and their survival.